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IL-10 induces apoptosis in human monocytes involving the CD95 receptor/ligand pathway

M Schmidt1, N Lügering, H G Pauels

  • 1Department of Medicine, University of Münster, Germany.

European Journal of Immunology
|July 18, 2000
PubMed

Insights

Interleukin-10 (IL-10) induces programmed cell death (apoptosis) in human monocytes. This IL-10 effect involves the CD95 receptor/ligand system, contributing to its anti-inflammatory properties.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Interleukin-10 (IL-10) is a potent immunosuppressive cytokine.
  • The precise mechanisms underlying IL-10's anti-inflammatory actions are not fully understood.

Purpose of the Study:

  • To investigate the effects of IL-10 on human peripheral blood monocytes.
  • To elucidate the molecular pathways involved in IL-10-mediated monocyte apoptosis.

Main Methods:

  • Monocyte apoptosis was assessed using annexin-V staining, TUNEL assay, electron microscopy, and DNA laddering.
  • Caspase activity was evaluated, including the role of caspase-8.
  • Expression of the CD95 receptor and ligand was analyzed following IL-10 treatment.
  • The impact of a CD95 ligand-neutralizing antibody on IL-10-induced apoptosis was determined.

Main Results:

  • IL-10 dose- and time-dependently induced apoptosis in human monocytes.
  • IL-10-induced apoptosis was dependent on caspase activation, specifically caspase-8.
  • IL-10 treatment led to increased surface expression of CD95 receptor and ligand on monocytes.
  • Neutralization of CD95 ligand significantly inhibited IL-10-induced monocyte apoptosis.

Conclusions:

  • IL-10 triggers monocyte apoptosis through a mechanism involving the CD95 receptor/ligand system.
  • This apoptosis pathway may operate via autocrine or paracrine signaling.
  • Induction of monocyte apoptosis is a significant contributor to IL-10's anti-inflammatory effects.

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